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Is invasive aspergillosis hospital or community acquired: reassessing the evidence?

Is invasive aspergillosis hospital or community acquired: reassessing the evidence?. Malcolm Richardson PhD, FIBiol, FRCPath Department of Bacteriology & Immunology University of Helsinki.

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Is invasive aspergillosis hospital or community acquired: reassessing the evidence?

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  1. Is invasive aspergillosis hospital or community acquired: reassessing the evidence? Malcolm Richardson PhD, FIBiol, FRCPath Department of Bacteriology & Immunology University of Helsinki

  2. Are systemic fungal infectionshospital or community acquired?Re-assessing the evidence using invasive aspergillosis as a model

  3. Key issues • Air as a source of human infection • Water as a source of human infection • Other environmental sources of human infection • Hospital versus community acquisition of infection • Molecular strain typing of Aspergillus species

  4. Air as a source of human infection • Inhalation: most common portal of entry • Temporal association between hospital-based outbreaks and construction • Very little data on base-line concentrations • Longitudinal studies show no correlation between sporadic cases of IA and changes in spore count

  5. Where are patients exposed?

  6. Nosocomial aspergillosis

  7. Nosocomial aspergillosis

  8. Acceptable levels • HEPA filtered air: 0 • Open ward:? • General hospital areas: ? • Outdoor air: highly variable/seasonal

  9. Sources of Aspergillus spp. • Environment • Food • long list! • Sharing of salt and pepper pots • autoclave pepper • standing water • ice-making machines • fomites • carpets/furniture/fabrics/soft toys

  10. Fungal contamination of food distributed to neutropenic patients Food Contaminated Fungi samples (%) Tea 100 A. fum, A. flavus Pepper 100 A. fum, A. niger Freeze-dried soup 20 A. fum, A. niger Apricot 66 A. fum, A. flavus Kiwi 50 A. fum Banana 25 A. fum Grapefruit juice 15 A. fum Bouakline et al. JCM 2000; 38: 4272-4273.

  11. An outbreak of aspergillosis in a general ITU • 5-month period • 6 patients colonised • invasive infection in 2 • source of infection • dust • ceiling insulation material • dust falling through perforated false ceiling tiles Humphreys et al., JHI 1991

  12. Hospital water as a source of human infection • Aspergillus has been recovered from hospital water supplies • No definitive proof that water is a source of infection • Key issues: • Bioaerosols • Showerheads

  13. Water as a source of filamentous fungi in a childhood bone marrow transplantation unit • 168 filtered water samples • 20 water-related surfaces: swabbed • Moulds recovered from all water samples • Aspergillus fumigatus • 60% taps • 75% main water supply • Water-related surfaces: 25% positive for moulds (only 2 samples positive for A. fumigatus) Warris et al. JHI 2001; 47: 143-148.

  14. Refinements of environmental assessment during an outbreak investigation of IA in a leukemia and BMT unit Study stresses • adequate pressure differentials between corridors and patient rooms • double-door entry into patient rooms • HEPA filtration • large-volume (1, 200 L) sampling superior Chloe et al. Infect Control Hosp Epidemiol 2000; 21: 18-23.

  15. Efficacy of prevention by HEPA filtration or laminar airflow against Aspergillus airborne contamination during hospital renovation • Strong association between building renovation and an increase in environmental contamination • Confirmation of the high efficacy of laminar airflow plus HEPA filtration and a high air-exchange rate • HEPA filtration alone did not prevent contamination during renovation • ”A standard protocol for aerobiological surveillance is needed” Cornet et al. Infect Control Hosp Epidemiol 1999; 20: 508-513.

  16. Concentrations of airborne Aspergillus compared to the incidence of invasive aspergillosis: lack of correlation • 54-week air sampling period • A. fumigatus and A. flavus: mean 1.83 cfu m-3 • Individual samples: maximum: 11.6 cfu m-3 • No correlation with season or ward • 6 cases of IPA during sampling period • No association with fluctuations in air count Conclusion: “the available data do not provide a firm link between hospital exposure and an increased incidence of aspergillosis” Hospenthal et al., Medical Mycology 1998.

  17. Hospital versus community acquisition of infection • Most cases sporadic • Incubation period unknown • No definition of hospital-acquired IA • Minimum time limit: 3, 4, or 7 days after admission • Hospital air becomes contaminated: but outbreaks uncommon

  18. Aspergillus: Time to diagnosis of aspergillosis after BMT Graft versus host disease 20 18 16 14 12 10 8 6 4 2 0 Neutropenia Wald et al. J Infect Dis 1997;175:1459 (modified by J.P. Donnelly) Cases 10 20 30 40 50 60 70 80 90 100 110 120 130 140 150 160 170 Days after transplant

  19. HSCT: changing timescale of IA 53% p=0.09 1987-93 30% 1993-98 % 17% p<0.001 Time after SCT (1993-98) Marr et al Blood 2002; 100: 4358-66. Slide courtesy of B.L. Jones

  20. Hospital-acquired IADefinition “A case of IA occurring more than 7 days after admission, or less than 14 days after discharge” During 2-year construction period >70% of IA cases acquired outside hospital setting Patterson et al. 1997; Infect Control Hosp Epidemiol 18: 104-108.

  21. Are patients colonised before admission? The evidence • PCR data • Screening • Tissue biopsies

  22. Are patients colonised before admission? Prediction of invasive pulmonary aspergillosis from colonization of lower respiratory tract before BMT • 134 patients: 2 BALs at time of transplantation • 7/134 PCR positive for Aspergillus • 5/7 developed IPA median 64 days after Tx Study suggests that IPA patients were colonised before Tx Einsele et al. 1998 Lancet.

  23. Are patients colonised before admission? • 121 patients admitted for cancer chemotherapy - no SFI • Screened by PCR - whole blood • 28/121 (23%) Aspergillus DNA positive

  24. Are patients colonised before admission? Pulmonary Aspergillus colonization in humans and its impact on management of critically ill patients • 56 patients undergoing thoracic surgery • Lung tissue samples • 63% evidence of pulmonary fungal colonisation • 39% Aspergillus Lass-Florl et al Brit J Haematol 1999.

  25. Late onset of IA in BMT patients at a university hospital • 93 allogeneic and 149 autologous pts • 20 month period • 0% IA autologous • 15.1% allogeneic: overall incidence 5.8% • Median time to occurrence: 92 days • No de novo cases prior to engraftment • Survival 100 days from diagnosis 29% • Conclusions • shift towards late occurrence • outpatient environment surveillance Grow et al., BMT 2002; 29: 15-19

  26. Invasive mold infections in allogeneic BMT recipients • 94 adult patients • 15 cases invasive mould infections: • A. fumigatus 7/15 (47%) • Aspergillus species 5/15 • Median time to onset: 102 days (18-470) “Although these data suggest community rather then nosocomial acquition because of the late timing of clinically evident disease, the source of these pathogens remains speculative because detailed epidemiological surveys were not conducted during the study period” Baddley et al. CID 2001; 32: 1319-1324.

  27. Surveillance of the home environment

  28. Patients live in mouldy houses:exposure to Aspergillus and more

  29. Patients live in mouldy houses and are exposed to Aspergillus fumigatus

  30. Late-onset IA Aspergillosis: the most common community acquired pneumonia with gram-negative bacilli as copathogens in stem cell transplant recipients with GVHD • 88 allogeneic HSCT: GVHD/corticosteroids • 12 patients hospitalised with pneumonia • 10/12 pulmonary aspergillosis: CT scan diagnosis • 6/10 bacterial copathogen “Aspergillosis is the most common cause of community-acquired pneumonia among allogeneic HSCT with GVHD. CT must be used to exclude an underlying fungal cause in patients who present with a gram-negative pneumonia” Alangaden et al. CID 2002

  31. Molecular typing studies • 21 environmental isolates • 26 clinical isolates • Genotyping RAPD • 34 distinct profiles • 2 cases: genetic similarity • J Hosp Infect 2005; 60: 61-68

  32. Prevention is better than cureAvoid exposure in the hospital and in the home

  33. Prevention is better than cure • avoidance of exposure • prospective surveillance: standard protocol: • hospital environments • home/workplace environments • prophylaxis • patient screening: nasal swabs/BAL • Galactomannan ELISA • PCR

  34. Key references Warnock DW, Hajjeh RA, Lasker BA. Epidemiology of invasive aspergillosis. Curr Infect Dis Rep 2001; 3: 507-516. Hajjeh RA, Warnock DW. Counterpoint: invasive aspergillosis and the environment – rethinking our approach to prevention. Clin Infect Dis 2001; 33: 1549-1552. Richardson MD. Changing patterns and trends in systemic fungal infections. J Antimicrob Chemo 2005 (in press).

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